Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paediatrics > GI > Flashcards

GI Flashcards

1
Q

Define GORD
What is the cause?
Which age is most affected?

A
  • Involuntary passage of gastric contents into the oesophagus
  • caused by relaxation of the lower oesophageal sphincter due to functional immaturity
  • affects 0-12 month olds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which group of children is GORD most common in?

A
  • cerebral palsy or other neurodevelopmental disorder
  • preterm esp. with bronchopulmonary dysplasia
  • Following surgery for oesophageal atresia or diaphragmatic hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are potential complications of GORD?

A
  • Faltering growth
  • Oesophagitis –> hematemesis, discomfort on feeding or heartburn, iron deficinecy anaemia
  • recurrent pulmonary aspiration - recurrent pneumonia, cough, wheeze, apnoea
  • dystonic posturing (sandifer syndrome)
  • life threatening events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is GORD diagnosed and which investigations can be done?

A
  • usually diagnosed clinically
  • 24 hr oesophageal pH monitoring to quantify degree of reflux
  • 24 hr impedance monitoring
  • endoscopy with oesophageal biopsies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the management of GORD?
uncomplicated
significant
and failure to respond?

A
  • uncomplicated - reassure parents, add thickening agent to feed, smaller more frequent feeds
  • significant - H2 receptor antagonist (ranitidine) or PPI (omeprazole)
  • fails to respond - consider other diagnosis e.g cows milk protein allergy
    unresponsive to medical - Nissen fundoplication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the cause of pyloric stenosis in children?

A

hypertrophy of pyloric muscle causing gastric outlet obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Who does pyloric stenosis mostly

affect?

A
  • babies 2-8 weeks

more common in:

  • boys
  • first borns
  • could be familial history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the features of pyloric stenosis?

A
  • Vomiting, can be projectile
  • peristaltic wave and palpable mass after feeding
  • hunger and dehydration
  • weight loss
  • Hypocholaraemic metabolic alkalosis
  • low plasma Na+, Low K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you diagnose Pyloric stenosis?

A
  1. Test feed - palpable mass RUQ, Gastric peristalsis
  2. if stomach over-distended with gas, empty with NG tube
  3. US - helpful to confirm diagnosis pre surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do you manage pyloric stenosis?

A
  1. IV fluids to correct electrolyte imbalance

2. Ramsted Pyloromyotomy - division of hypertrophied muscle down to mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms of acute appendicitis?

A
  • anorexia
  • vomiting
  • Abdo pain - inititally central and colicky –> localizing to RIF (from localised peritoneal inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the signs of acute appendicitis?

A
  • Fever
  • Abdo pain (worse on movement)
  • persistent tenderness and guarding of RIF (McBurneys point)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is intussusception?
Where is the commonest site?
Which age does it affect the most?

A
  • invagination of proximal bowel into a distal segment.
  • most common is ileum into caecum at the illeocaecal valve
  • 3 months - 2 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some complications of intussusception?

A
  1. stretching and constriction of mesentry
    leading to venous obstruction leading to engorgement and bleeding from bowel mucosa
  2. fluid loss
  3. bowel perforation
  4. peritonitis
  5. gut necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the symptoms of intussusception?

A
  1. paroxysmal, severe colicky pain with pallor- during pain episode child is pale, draws up legs
  2. Lethargy between episodes
  3. refuse feeds
  4. vomiting- bile stained depending on site of intussusception
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the signs of intussusception?

A
  1. Sausage-shaped mass- palpable
  2. Characteristic passage of redcurrant jelly stool comprising blood-stained mucus- may be seen on rectal exam or late sign
  3. Abdominal distention or shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the investigations of intussusception and what do you see in each?

A
  • X-ray abdomen- distended small bowel and absence of gas in the distal colon or rectum
  • Abdominal USS- confirms diagnosis (target/doughnut sign)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the management for intussusception?

A
  • IV fluid resuscitation immediately, as there is often pooling of fluid leading to hypovolaemic shock
  • Reduction of intussusception by recta air insufflation – risk of bowel perforation
  • Remaining 25% that are unsuccessful or where peritonitis present then –> operative reduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is Meckels Diverticulum?
How does it present?
What is the investigation and what does it show?
What is the treatment?

A
  1. congenital defect, ileal region, left over from umbilical cord
  2. usually asymptomatic, can present with
    • acute Hb decrease,
    • bleeding which can be life threatening - characteristically neither bright or malaena,
    • intussuception, volvulus
  3. technetium scan - shows uptake by gastric mucosa
  4. Tx = surgical resection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two types of malrotation?
When does it usually present?
What can happen in volvulus?

A
  1. obstruction or obstruction with compromised blood supply
  2. tends to present first 1-3 days of life but can present at any time
  3. mesentery not fixed - rotation can cause superior mesenteric arterial blood supply to small intestine and proximal large intestine to be compromised –> infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the presentation of volvulus?
What is the investigation?
What is the treatment?

A
  1. billous dark green vomit, abdo pain, tenderness from peritonitis or ischaemic bowel
  2. urgent gastro contrast study (indicated if billious vomiting)
  3. treatment - urgent surgical correction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When does cows milk allergy typicall occur and in children being fed what?
Which immune reactions are at play?
Which type of cows milk allergy is each immune reaction associated with?

A
  • first three months of life, usually in formula fed infants
  • Immediate (IgE mediated) and delayed (non-IgE mediated)
  • Immediate - Cows milk protein allergy, delayed - cows milk protein intolerance
23
Q

What symptoms do children with cows milk allergy present with?
How is the diagnosis made?
How do you manage cows milk protein allergy?
when do kids improve?

A
  • regurgitation and vomiting
  • diarrhoea
  • urticaria, atopic ecxma
  • colic symptoms: instability, crying
  • wheeze, chronic cough
  • rarely: angioedema, anaphylaxis

Diagnosis:

  • often clinical - challenge test/imrpovement on removal of cows milk
  • skin prick/patch test
  • total IgE and specific IgE (RAST) for cows milk protein

Management:

  • forumala fed - give extensive hydrolysed formula milk if not working, try amino acid based milk
  • breastfed - cut out cows milk from maternal diet, give calcium supplements. not working, given extensive hydrolysed formula milk
  • CMPA - 50% recover by age 5
  • CMPI - usually by age 3
24
Q

What are the causes of gastroenteritis and how do they present?

A
  • Bacterial causes
    • presence of blood in stools, campylobacter jejuni most common
    • shigella and salmonella: dysenteric infection, blood and pus in stool, pain and tenasmus, high temps
    • cholera and enterotoxigenic E.coli : profuse rapidly dehydrating diarrhoea

Protozoan: Giardia and cryptosporidium
Giardiasis: protzoan have cystic form in stoolm motile trophozites in small intesntine, villous atrophy with IgA deficiency, diagnosis by cysts in stool. Treat - 3/6 high dose metroniadazole

25
Q

How does gastroenteritis typically present, what can it follow, and what can it lead to in severe cases?

A

In gastroenteritis: sudden change to loose or watery stool with vomiting

  • can be following contact with diarrhoea, recent travel
  • dehydration can lead to shock
26
Q

Who is at increased risk of dehydration in gastroenteritis?

A
  • infants >6 months due to greater surface area to weight ratio, those with low birthweight
  • > 6 diarrhoeal stools in past 24 hrs
  • > 3/4 vomits in last 24 hrs
  • unable to tolerate extra fluids
  • malnutritioned
27
Q

How do you assess dehydration in gastroenteritis?

A

most accurate = degree of water loss
• No clinically detectable dehydration (usually <5% loss of body weight)
• Clinical dehydration (5-10% loss of body weight)
• Shock (>10% loss of body weight)

28
Q

Define isonatraemic and hyponatraemic dehydration and what is the risk in the latter?

A
  1. Isonatraemic: loss of water and sodium is proportionall
  2. Hyponatraemic: when children with diarrhoea drink lots of water, greater net loss of sodium. leads to shift of water from extracellular to intracellular compartments.
    - risk of increased brain volume leading to seizures
29
Q

What is hypernatraemic dehydration and what are the

  • causes
  • presentation
  • risk
  • what else occurs?
A
  • where water loss exceeds relative sodium loss and concentration increases
  • caused by insensible water losses - high fever, hot dry environments or from profuse low sodium diarrhoea
  • fluid shifts from intracellular space
  • presentation: depression of fontanelle, sunken eyes, reduced skin elasticity
  • risk of water beinf drawn out of brain leading to
    • cerebral shrinkage,
    • jittery movements
    • increased muscle tone, hyperreflxia
    • altered consciousness
    • seizures
    • multiple cerebral haemorrhages
  • transient hyperglycaemia, self correcting.
30
Q

Investigations for Gastroenteritis

Management

  • normal
  • other meds?
  • abx?
A

Stool culture if septic/blood mucus in stool/immunocompromised
Plasma electrolyes, urea, creatinine and glucose

Management

  • oral rehydration therapy if clincially dehydrates
  • IV only if shock or deterioration or persistent vomiting
  • avoid fruit juices/carbonated drinks
  • in hypernatraemic dehydration: slow, ideally oral but IV at least over 48hr due to risk of rapid drop of plasma osmolality leading to cerebral odeama - seizures
  • no medications for vomiting and diarrhoea
  • abx only if septic, spread of infection, salmonella under 6 months, immunocompromised/malnutritioned
  • increase nutritional intake
31
Q

What is IBS?

the presentation of IBS?

A
  • Altered GI motility and abnormal sensation of intra-abdominal events

Presentation

  • non specific abdo pain - often periumbilical, may be improved on defecation
  • bloating
  • explosive loose or mucousy stool
  • feeling of incomplete defecation
  • constipation (often alternating with normal/loose stool)
32
Q

What is Coeliac disease? where does ut occur, cause? what does it lead to>
What is the genetic association?
What does it lead to?

A
  • gluten sensitivity enteropathy where gliadin component and other prolamines leads to immune response
  • occurs in proximal small intestine mucosa
  • leads to cell loss from villous top leading to flat mucosa
  • Genetics: Class 2 Human leukocyte antigen (HLA) molecules DQ2* and DQ8
33
Q

What are the risk factors of coeliac disease?

What is the presentation?

A
  1. T1DM
  2. Thyroid disease
  3. Downs syndrome
  4. Family Hx
  5. Short stature
  6. IgA deficiency

Presentation

  • at 8-24 months on intro of wheat containing foods
  • faltering growth
  • abdo distension
  • buttock wasting
  • anaemia (iron and folate)
  • abnormal stools
  • general irritability
  • dermatitis herpetiformis
  • dental enamel defects
34
Q

What investigations for coeliac disease? what do they show

What is the criteria?

What is the management?
what are the risks if non adherent

A
  • Positive serology- anti-tTG, EMA (endomysial antibodies)
  • Mucosal changes (increased intraepithelial lymphocytes, villous atrophy, crypt hypertrophy) on small intestinal biopsy. Resolution of symptoms and catch-up growth upon gluten withdrawal

criteria-
o Characteristic histology (Marsh type III a - c)
o Positive serology
o Symptomatic response to gluten exclusion
o Resolution of antibodies

Management
• All products containing wheat, rye, barley removed from diet
• Dietician supervision
• Gluten challenge later on to show continuing susceptibility
• Risk of osteopenia, osteoporosis, bowel malignancy (small bowel lymphoma) if non-adherent to diet

35
Q

What is chronic non specific diarrhoea/toddlers diarrhoea?
when does it present? when does it resolve?
what are possible causes?

How does it present?

A
  • persistent loose stool in preschool children
  • onset 6-20 months, usually resolves by age 3
  • can be due to excessive fruit juice
  • can be temporary cows milk allergy after gastroenteritis
Presentation
•	*Normal growth*
•	3-4 stools per day 
•	1st stool of day is large, others small 
•	*Stools contain mucus + undigested food*
•	Diarrhoea recurrent or persistent 
•	No relation to diet 
•	F.H of functional bowel symptoms
36
Q

Which parts of the GI tract can Crohns affect?

is it more or less common than ulcerative colitis?

A

anywhere from mouth to anus

more common than UC

37
Q

How does Crohns present?

A
  • growth failure
  • abdominal pain, diarrhoea, weight loss
  • fever, lethargy
  • extraintestinal - oral lesions or perianal skin tags, uveitis, arthralgia, erythema nodosum
38
Q

How do you diagnose Crohns disease?

What is the hallmark?

A
  • Bloods - raised ESR/CRP, iron deficiency anaemia, low serum albumin
  • Endoscopic and histological findings on biopsy
  • hallmark : non-caseating epitheliod cell granulomata
  • stricture and fistula of the bowel may develop
39
Q

How do you manage Crohns disease?

A
  1. induce remission with nutritional therapy (replace diet with whole protein modular feeds - polymeric diet) for 6-8 weeks. If uneffective, use systemic steroids
  2. Maintain remission - immunosuppressant medication e.g Azathioprine, methotrexate
  3. If conventional treatment fails - TNF agents e.g infliximab, adalimumab
  4. Long term supplemental enteral nutrition - NG, gastrostomy
  5. surgery for complications - obstruction, ffistula, abscess formation, localised diseases unresponsive to medical treatment
40
Q

Which part of the GI tract does UC affect?

How does it present?

A

Mucosa of the colon alone

Presentation

  1. diarrhoea,
  2. rectal bleeding
  3. colicky abdominal pain
  4. weight loss, growth faltering
  5. extraintestinal - erythema nodosum, arthritis
41
Q

How do you diagnose UC? What are the findings?

A
  • endoscopy with biopsy
  • –> histological findings: mucosal inflammation, crypt damage (loss, abscesses, distortion) and ulceration
  • confluent colitis extending from rectum proximally
  • 90% have pancolitis
42
Q

How do you manage Ulcerative Colitis?
mild

disease confined to rectum and sigmoid colon

more extensive/aggressive

A

Mild Disease
- aminosalicylates e.g Mesalazine: for induction and maintenance

Disease confined to rectum and sigmoid colon: topical steroids

More extensive or aggressive: systemic steroids for acute exacerbations + Azathioprine to maintain remission or in combination with low dose corticosteroids

resistant disease - biological : infliximab or ciclosporins

Severe fulminating disease complicated by toxic megacolon: colectomy with ileostomy or ileorectal pouch

43
Q

What does UC increase risk of as an adult and what has to be done routinely?

A
  • increases risk of adenocarcinoma of colon

- reiagnosisgular colonscopic screening is performed after 10 years from d

44
Q

What is normal bowel motions for a newborn? for a 1 year old? for a breastfed baby?

A
  • 4 bm per day for newborn
  • reduces to 2 per day by 1 year
  • breasted infants may have none for several days
45
Q

What is the definition of constipation?

A
  • infrequent passage of dry, hardened faeces often accompanied by straining or pain and bleeding associated with hardened stool
  • may be abdo pain
46
Q

What are the possible precipitating factors of constipation and causes in older children?

A

constipation could be precipitated by

  • dehydration/reduced fluid intake
  • anal fissure causing pain

older children

  • problems in toilet training
  • refusal/anxiety about opening bowels at school or in unfamiliar toilets
47
Q

What do each of the following red flag signs suggest could be the cause of contipation?
1. failure to pass meconium within 24hrs of life

  1. Faltering growth
  2. Gross abdominal distention
  3. Abnormal lower limb neurology or deformity e.g talips (clubfoot) or secondary urinary incontinence
  4. sacral dimple above natal cleft, over the spine - naevus, hairy patch, central pit
  5. Perinal fistula, abscesses, fissures
A
  1. Hirschsprung disease
  2. hypothyroidism, coeliac disease,
  3. Hirschsprung disease or other gastrointetstinal dysmotility
  4. Lumbosacral pathology
  5. Spina Bifida Occulta
  6. Crohns disease
48
Q

What may happen in long standing constipation?

A
  • the rectum may become over distended leading loss of feeling of urge to defecate,
  • involuntary soiling may occur as contractions of the full rectum inhibit the internal sphincter leading to overflow
49
Q

Management of overflow diarrhoea ?

A
  1. initital aim is disimpaction - regimen of stool softeners (macrogel laxative e.g polyethylene glycol + electrolytes).
  • escalating dose regiment over 1-2 weeks
  • if unsuccesful - stimulant laxatives can be used
  1. maintenance using macrogel laxative
50
Q

What is the cause of Hirschsprungs disease?

where is the majority confined to?

A
  • absence of ganglionic cells in myenteric and submucosal plexus in part of the large bowel resulting in narrow contracted segment
  • 75% confined to rectosigmoid
51
Q

What is the presentation of Hirschsprungs disease?

A
  1. neonatal obstruction leading to failure to pass meconium in first 24 hours of life
  2. abdominal distension
  3. bile stained vomit
  4. rectal exam- narrow segment and removal = gush of liquid and flatus
  5. later in life constipation, abdo distension with no soiling
  6. growth failure may be present
52
Q

How is Hirschsprungs disease diagnosed?

A
  • suction rectal biopsy (absence of ganglion cells)
53
Q

What is the management of Hirschprungs disease?

A

surgical - initial colostomy followed by anastomising normally innervated bowel to the anus

Paediatrics (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions